Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Cns > metabolic > Flashcards

metabolic Flashcards

1
Q

In ethanol toxicity what will the patient present like?

A

withdrawl symptoms: tremor, tachycardia, HTN, malaise, nausea,DTs
physiologic tolerance, dependence

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What are some direct effects of ethanol toxicity?

A

cerebellar vermis atrophy (ataxia)
loss of purkinje cells
Bergmann’s gliosis in cerebellum

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What are some indirect effects of ethanol toxicity?

A

vitamin deficiency with Werniecke’s or Korsakoff
liver cirrhosis…hyperammonemia
…..hepatic encephalopathy
cerebral trauma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

How is ethanol toxicity diagnosed?

A

clinical presentation and patient history (CAGE)

blood alcohol levels

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What is the treatment for ethanol toxicity

A

avoid alcohol, disulfram to condition patient to abstain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What are some possible complications of ethanol toxicity?

A

Werniecke-Korsakoff, liver cirrhosis, hepatic encephalopathy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What cell is seen in increased levels in the cerbrocortical tissue in hepatic encephalopathy?

A

astrocytes(responsible for removing ammonia by converting to glutamine)
excess ammonia in systemic bc of hepatic resistance

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What is the etiology of hepatic encephalopathy?

A

metabolic toxicity of the brain due to increased portosytemic shunt

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What is associated with hepatic encephalopathy?

A

70% of patients with cirrhosis have subtle HE signs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What is the pathophysiology of HE?

A

1.increased hepatic resistance so portosystemic shunt
2.increased ammonia levels in brain and body
astrocytes damaged because of increased ammonia
3.astrocytes cannot convert ammonia to glutamine
AND
1.increased production of endogenous benzodiazepene…2.increased GABA content of brain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What is the presentation of HE?

A
  1. initially confused, derangement of consciousness, increased psychomotor activity
  2. eventually -drowsy, stupor, coma
    - asterixis: intermittent muscle contract when attempt postural fixation
    - focal or general seizure
    - grimace, suck, grasp reflex present
    - exaggerated DTR, asymmetric DTR
    - Babinski
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What are some potential causes of subacute combined degeneration?

A

diet-starvation, eating disorder

exposure to NO gas

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What is the presentation of subacute combined degeneration?

A
  1. paresthesia legs, hands, feet symmetrical diffuse
  2. ataxia
  3. pernicious anemia
    progresses to
  4. motor: spastic weakness diffused and symmetrical
  5. dementia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What can vitB12 deficiency present like?

A

spinal myelopathy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

what is the etiology of subacute combined degeneration?

A

DC and LC of spinal cord are demylinated

motor is eventually demylinated too

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

what happens to myelin in subacute combined degeneration?

A

vacoulation
myelin is destroyed -astrocytosis
interstitial edema occurs because of osmotic change

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What is the treatment for Subacute combined degeneration

A

vitB12

recovery may be reversible but if complete parapalegia then recovery is poor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

what is the etiology of subacute combined degeneration?

A

cant absorb vit B12 across intestine wall

-effects on blood cell development and myelin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What are some causes of thiamine vit b1 def?

A 
starvation
dietary problems
hyperemesis
renal dialysis
cancer
AIDS
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

what type of neurodisease is vit B1 deficiency?

A

peripheral neuropathy

metabolic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

what is the pathophysiology of thiamine deficiency?

A
  1. thiamine not coming from diet as it should
  2. thiamine is a cofactor needed to produce ATP
  3. osmotic potentials change
  4. hemorrhage and necrosis around 3rd ventricle structures
  5. macros infiltrate lesions
  6. lesions become cystic
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What is the presentation of thiamine deficiency?

A

cardiopathy
peripheral neuropathy
encephalopathy
can develop into Wernieckes then develop further into Korsakoffs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What is the treatment for thiamine deficiency?

A

medical emergency, vit B1 supplements

Korsakoff’s may remain, all else is reversible

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

what population is likely to get thiamine deficiency?

A

alcholics

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What is the most common cause of Werniecke’s and Korsakoff’s syndrome?

A

alcholism

3% of alcoholics have either

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

what are some causes of Werniecke/Korsakoff?

A

similar to thiamine def.

hyperemesis, starvation, eating disorders, renal dialysis, AIDS, cancer

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

What is the pathophysiology of Werniecke/Korsakoff?

A

thiamine needed at cofactor for ATP production
hermmorage and lesion around 3rd ventricle structures (hypothal, thal, mammilary bodies, colliculi), infiltrate with macros, lesion turns cystic
(same as vit B1 thiamine def)
leads to memory loss, confusion, ataxia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

What is the presentaiton of Werniecke’s syndrome?

A

confusion, opthalmopelgia (lateral rectus or lateral gaze) and gait ataxia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

What is the presentation of Korsakoff’s?

A

confabulation, memory loss (learning and retention)

can progress from Werniecke’s

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

How is werniecke’s and Korsakoff’s diagnosed?

A

MRI: should see widening of 3rd ventricle and atrophy of paraventricular thalamus
vestibular testing
CAGE screen for alcholics

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

How is Werniecke’s and Korsakoff’s treated?

A

medical emergency thiamine
avoid alcohol
recovery from Korsakoff’s might not happen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

What are some complications to think about in Werniecke or Korsakoff’s syndromes?

A

liver failure
systemic infection
ethanol toxicity
alcohol withdrawal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

what is the etiology of Wilson’s?

A

genetic mutation of ATP7B gene
autosomal recessive
Cu transport ATPase protein defect

34
Q

What is the presentation of Wilson’s?

A

1.behavioral disturbance may present first
2.yellow green ring around cornea
3.liver signs
autonomic:BB incontinence, sweating, orthostatic hypotension
4.BG signs: dystonia, tremor, incoordination
dementia
migraine, seizure

35
Q

where does the Cu accumulate since it cannot be transported in Wilson’s disease?

A

liver and basal ganglia

36
Q

What is the treatment for Wilson’s

A 
chelating agent -penicillamine
liver transplant (curative)
37
Q

How is Wilson’s diagnosed?

A
  1. low serum ceruplasmin (protein that carries Cu in blood)
  2. eye rings
  3. MRI lesions high intensity on T2 (cell loss and gliosis)
  4. Cu toxicity in tissue
  5. genetic test
38
Q

What is the pathophysiology of Wilson’s?

A
  1. mutation in ATPB7 gene
  2. no ATPase to transport Cu
  3. failure at biliary excretion of CU
  4. Cu accumulate in BG and liver
  5. BG: dementia, tremor, incoordination
  6. Hepatic: hepatitis, cirrhosis, failure
39
Q

what increases the liklihood of Wilsons?

A

co-sanguinous populations
US heterozygote carrier 1/100
Japan has higher incidence

40
Q

what are some complications to think about in Wilson’s?

A

higher rate of natural abortions during pregnancy
can develop Werniecke-Korsakoff
liver cirrhosis, hepatic encephalopahty

41
Q

what type of neuropathy is diabetic neuropathy?

A

metabolic
sensorineural
peripheral

42
Q

What is the most common cause of peripheral neuropathy worldwide?

A

diabetic neuropathy

43
Q

What some metabolic sensorineural neuropathies?

A

Diabetic (chronic only becomes motor) (lose pain)
Thiamine
Thallium
Cisplastin (pain preserved)
(vit B12 subactute combined degen mostly sensory much later can become motor)

44
Q

After 25 years with diabetes, what percentage have diabetic neuropathy?

A

50%
upon diagnosis, 8% have some subtle signs
6.5% prevalence in US

45
Q

What are the 4 pathways believed to be involved in diabetic neuropathy?

A

polyol pathway increase
hexoamine pathway increase
glycolation pathway increase
PKC increase activity so more proinflamm

  1. leads to increase in free radicals and decrease in scavengers
  2. Vascular insufficiency
46
Q

What is the etiology of diabetic neuropathy

A
  • metabolic uncontrolled glucose levels
  • vascular insufficiency so lose of small fibers
  • and segmental demylination-axonopathy
47
Q

what are some rare presentations of diabetic neuropathy?

A

autonomic
focal or multifocal asymm neuropathy
small fiber and painful neuropathy
regional neuropathic syndrome

48
Q

What are the signs of classic diabetic neuropathy?

A

sensorineural peripheral

  1. numb tingle painless distal extremities
  2. pain worse at night begins in toes then up to calves then fingers and then arms
  3. chronic: motor weakness distal and atrophy
  4. chronic decreased DTRs
  5. sometimes autonomic dysfunction
49
Q

How is diabetic neuropathy diagnosed?

A

clincial findings, conduction studies not definitive, biopsy not usually

50
Q

what are some complications to think about with diabetic neuropathy?

A 
pain control: TCA, tramadol, anticonvulsants, narcotics
foot ulceration (foot hygiene)
51
Q

what is the treatment for diabetic neuropahty?

A 
none really (manage blood levels glucose) 
free rad scavengers not very helpful
52
Q

what is the presentation of cisplatin neuropathy?

A
  1. lose 2 PV
  2. pain retained
  3. paresthesia extremities
  4. lose hair cells
53
Q

What type of neuropathy is cause by cisplatin?

A

sensorineural metabolic peripheral

54
Q

what is the pathophysiology of cistplatin neuropathy?

A

axon degeneration

kills DRG in does dependent manner

55
Q

what is the most common toxic neuropathy in the US?

A

anticancer drugs like cistplatin

56
Q

what is the temporal profile of alcohol neuropathy?

A

progressive slow

57
Q

what type of neuropathy is alcohol neuropathy?

A

peripheral sensorimotor

58
Q

what are some common sensorimotor peripheral neuropathies?

A

alcohol, Hg, Arsenic, thiamine (vitb12 starts out sensory but can progress to motor) (diabetic starts sensory but chronic can become motor)

59
Q

What are some common motor peripheral neuropathies?

A

Pb

60
Q

What is the presentation of alcoholic neuropathy?

A
  1. burning paresthesias
  2. painful cramps
  3. weakness, wasting
    Stocking glove pattern for impaired 2 PV and PT
61
Q

What is the most common heavy metal neuropathy?

A

arsenic

62
Q

What is the pathophys of alcholic neuropathy

A

demylination
axonopathy
remits with abstinence

63
Q

What are some common presentations of heavy metal peripheral neuropathies?

A

encephalopathy, peripheral neuropathy

64
Q

How does lead heavy metal neuropahty present?

A

motor neuropathy

  1. UE weak> LE weak
  2. distal symmetric
  3. late stage-autonomic involvement
65
Q

how does mercury heavy metal neuropathy present?

A

sensorimotor

  1. exposure: industrial, dietary, dental amalgam
  2. distal
66
Q

How does thallium heavy metal neuropahty present?

A

sensorineural

  1. exposure: pesticides, rodenticides, industria, diet
  2. distal, symmetric
  3. mostly sensory large fibers 2PV axonopathy
  4. late state-autonomic
67
Q

how does arsenic heavy metal neuropathy present?

A

sensorimotor. slow onset
1. exposure: drinking water, intentional, industrial
2. symm
3. burning paresthesias initially
4. LE weakness> UE weakness
5. lose DTRs

68
Q

Which toxic metals cause axonopathy?

A

thallium, Arsenic, cisplatin, thiamine

alcohol also does

69
Q

How can you differentiate alcoholic neuropathy and arsenic heavy metal?

A

both are burning, both are sensorimotor, both progressive slow onset
arsenic presents with LE weakness greater than Upper extremity. lose DTRS
alcholic presents with stocking glove paresthesia and painful cramps

70
Q

What is the temporal profile of arsenic neuropathy?

A

slow progressive

71
Q

What are the signs and symptoms of Thiamine B1 deficiency?

A

cardiopathy
encephalopathy W andK
neuropathy-sensorimotor

72
Q

What is the presentation of thiamine B1 neuropathy?

A

sensorimotor

  1. acute, subacute onset
  2. paresthesia stocking glove
  3. weakness in legs
  4. Lose DTRS
73
Q

How is thiamine deficiency diagnosed?

A

empiric threatment with oral Thiamine B1

74
Q

In a long standing alcoholic patient what would be found in cerbellum?

A

dead purkinje cells

Bergmann’s gliosis because glial cells proliferate due to dead purkinje cells

75
Q

On imaging of a Werniecke-Korsakoff patient what would you see?

A

widening of 3rd ventricle

atrophy of paraventricular thalamus

76
Q

What is a demylinating disease of the pons?

A

central pontine myelinolysis

77
Q

What patient population is likely to get CPM?

A

liver transplant
alcoholics (1/2 of cases)
renal dialysis

78
Q

what is the etiology of CPM?

A

rapid over correct for hyponatremia

79
Q

what is the presentation of CPM?

A
  1. acute to subacute
  2. loss of ability to use cranial nerves (can’t chew, swallow, speak)
  3. flaccid paralysis all 4 limbs
80
Q

What might be spared in CPM?

A

ocular movements and facial movements (pons and midbrain)

“locked in syndrome”

Cns (12 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions